Ch. 22, 23, 24 Flashcards
Uterine atony
failure of uterus to contract and retract after birth
What is usually responsible for primary/immediate pPh?
What is the cause for late/delayed ppH?
Immediatae - uterine atony
Delayed- lacerations, uterine inversion, subinvolution, rupture
Degree of shock
Mild - 20%
Symptoms
Diaphoresis, increased cap refill, cool extremeities, maternal anxiety
Degree of shock
Moderate 20-40%
Symptoms
Tachycardia, postural hypotension, oliguria
Degree of shock
Severe >40%
Symptoms
Hypotension, agitation/confusion, hemodynamic instability
Typical signs of hemorrhage do not appear until as much as ____ml of blood has been lost
1800-2100ml
Why are the typical signs of hemorrhage not noticed earlier in pregnancy?
Maternal bv increases as much as 50%. Plasma volume increases
All of this provides a reserve for the blood lost during delivery
What are causes for PPH
Laceration, episiotomy, retained placental frag, uterine inversion, coag disorder, large baby, failure to progress during 2nd stage of labor, placenta accreta, induction with oxytocin, surgical birth, hematoma
Overdistension of uterus can be caused by what
Mutliple gestation, macrosomia, hydramnios, fetal abnormality, placenta previa, precipitous birth, retained placental frag. Prolonged or rapid forceful labor, bacterial toxins, anesthesia (halothane) mag sulf
Subinvolution
incomplete involution of uterus or failure to return to its normal size and condition after birth
Complications of subinvolution
hemorrhage, pelvic peritonitis, salpingitis, abscess formation
Causes of subinvolution
Retained placental frag, distended bladder, excessive maternal activity prohibiting proper recovery, uterine myoma, infection
Clinical picture of subinvolution
Treatment
pp fundal height that is higher than expected, boggy uterus, lochia fails to change color
stimulating uterus to expel frag with uterine stimulant and antibiotics
Uterine inversion
treatment
top of uterus collapses into inner cavity due to excessive fundal pressure or pulling on imbilical cord when placenta is still firmly attached to fundus
Treatment uterine relaxants, immediate manual replacement
Uterine rupture symptoms
pain, fetal heart rate abnormalities, vag bleeding
How does thrombosis prevent PPH after birth
by providing hemostasis. Fibrin deposits and clots in supplying vessels
What are abnormal coagulation studies
decreased platelet and fibringogen levels
increased prothrombin time
partial thromboplastin time
Fibrin defradtion productions and prolonged bleeding time
Thrombotic thrombocytopenic purpura
define
therapy
Autoimmune disorder of increased platelet destruction
**Glucocorticoids and caplacizumab = therapy
Von Willebrand Disease
Symptoms?
Prolonged bleeding time, deficiency of von willebrand factor and impairment of platelet adhesion
Signs - bleeding gums, easy brusing, menorrhagia, blood in urine/stools, nosebleeds, hematomas
*Von Willebrand factor increases in most women during preg. so not affected
Disseminated intravascular coagulation
acquired coagulopathy - clotting system is abnormally activated, resuling in widespread clot formation in small vessels throughout body which leads to depletion of platelets and coag factors
*not itself an illnes, always a secondary diagnosis
Clincal features of DIC
Petechiae, ecchymoses, bleeding gums, fever, hypotension, acidosis, hematoma, tachycardia, proteinuria, uncontrolled bleedind during birth, acute renal failure
Treatment goals for DIC
Maintain tissue perfusion through aggressive fluid therapy, oxygen, heparin, blood products
*treatment recommended for at least 2 weeks post birth
If PP bleeding continues even if there are no lacerations, nurse should suspect?
Retained placental fragments
What are symptoms of hematoma
Uterus is firm with bright red bleeding
Localized bulging area just underskin in perineal area
Severe pain and diff voiding
Hypotension, tachycardia and anemia
What do these findings suggest?
Gingival bleeding, petechiae, ecchymosis, venipuncture sites are oozing and prolonged bleeding. Lochia greater than normal
Increase in pulse and decrease in level of consciousness
Urinary output diminished
Coagulopathy
Contraindications for
PITCOIN
Never give undiluted as a bolus injection IV
Setup as a piggyback to ensure med can be discontinued promptly
Contraindications for
CYTOTEC
(mistoprostol)
Allergy, active cardiovascular disease, pulmonary or hepatic disease / caution in moms with ASTHMA
Never give undiluted as bolus injection IV
Contraindications for
PROSTIN E2 (dinoprostone)
active cardiac, pulmonary , renal or hepatic disease
Contraindications for
METHERGINE
Hypersensitive and hyertension
Contraindications for
HEMABATE (CARBOPROST)
ASTHMA due to bronchial spasm
active cardiovascular disease, pulmonary, renal or hepatic disease
Superficial venous thrombosis
usually involved saphenous venous system
confined to lower leg
*may be caused by use of lithotomy position
DVT
Involves what veins
deep veins from foot to calf, thighs, pelvis’
More common in left lower extremity
Calf swelling and tender, difference in circumference, erhthemia, warmth, pain with pressure, pedal edema
*can dislodge and migrate to lungs causing PE (unexplained SOB, severe chest pain)
Signs of PE
unexplained SOB, chest pain, tachypnea, tachycardia, fever, hypotension, syncope, distention of jugular vein, decreased o2, cardiac arrhythmias, hemoptysis, sudden change in mental status
What is treatment for mom with superficial venous thrombosis
NSAIDs
rest and elevation of affected leg
Warm compress
Antiembolism stockings
Parametritis
extension of endometritis, involves broad ligament and possbily ovaries/fallopian tubes
inflammation of pelvic floor
Septic pelvis thrombophlebitis
Infection speads along venous routes into pelvis
Postpartum infection / signs and symptoms
Endometritis
Lower ab tenderness or pain
Temp elevation
Foul smelling lochia
Anorexia
Nausea
Fatique
Leukocytosis and elevated sedimentation rate
Postpartum infection / signs and symptoms
Wound infection
Weeping serosanguineous or purulent drainage
Separation of edges
Edema
Erythema
tenderness
Discomfort
Maternal fever
Elevated WBC
Postpartum infection / signs and symptoms
UTI
URgency
frequency
dysuria
flank pain
low grade fever
urinary retention
hematuria
urine positive for nitrates
cloudy urine with strong odor
Postpartum infection / signs and symptoms
Mastitis
Flu-like symptoms
Tender, hot, red painful area on one breast
inflammation
cracking of skin around nipple
breast distention with milk
Appropriate for gestational age (AGA)
newborn with weight that falls within the 10th to 90th percentile for gestational age
Small for gestational age (SGA)
Newborns that weight less than 2500g (5lb8oz) at term
*below the 10th percentile
Large for gestational age (LGA)
newborns whose birth weight is above 90th percentile, weighing more than 4000g (8lbs 13oz)
(LBW) low birth weight
Very low birth weight
Extremely low birth weight
(LBW) low birth weight - 2500g (5.5lb)
Very low birth weight - less than 1500g (3lb5oz)
Extremely low birth weight- less than 1000g (2lb)
Fetal growth restriction FGR
Also can be from?
pathologic counterpart of SGA
Rate of growth does not meet expected growth pattern
Placental insufficiency is principle cause of FGR
Can also result from aneuploidy, maternal malnutrition, htn, smoking, preE, chromosomal abnormalities, congenital malformations, infections
Prolonged or sustained neonatal hypoglycemia can lead to
brain injury
Polycythemia
Venous hematocrit above –%? and hemoglobin of more than –g?
-what happens? symptoms?
Venous hematocrit above 65% and hemoglobin of more than 20g
INcreased viscosity of blood assoc with symptoms of hypoperfusion / increased resistence to blood flow, decreased O2 delivery- can cause CNS dyfunction, hypoglucemia, decreased renal function, cardiorespiratory distress, coagulation disorders.
Clinical signs - respiratory distress, cyanosis, feeding diff, hypoglycemia, jitteriness, jaundice, ruddy skin color, seizures, lethargy
How to support newborns with polycythemia
Asymptomatic
Symptomatic
Asymptomatic - fluids, close observations, repeat hemtocrit in 12 hours
Symptomatic - partial exchange transfusion w/ replacement of removed red blood cell with normal saline
What are maternal factors that increase change of LGA newborn
DM, multiparity, prior history, postterm, obesity, gestational weight gain, male fetus, genetics
SIgns of hypoglycemia in newborn
Lethargy, apathy, drowisness, irritability, tachypnea, weak cry, temp instability, jitteriness, seizure, apnea, bradycardia, cyanosis, pallor, feeable suck, poor feeding, hypotonia and coma
**may present with similar findings: septicemia, severe respiratory distress, congenital heart disease
Hypoglycemia
below 35-45mg/dl
AAP recommends intervening for blood glucose less than 40 in 1st 4 hours of life and less than 45 at ages 4-24hrs
How to treat hypoglycemia
Asymptomatic
Symptomatic
Asymptomatic - supervised feeding
Symptomatic- freq feeding, dextrose gel massaged into buccal mucosa. If persist, IV dextrose
Treatment to
-Decrease blood viscosity
-lower hematocrit & blood viscosity
-hyperbilirubinemia
**Decrease blood viscosity **- increase fluid volume
lower hematocrit & blood viscosity - partial exchange transfusion
**hyperbilirubinemia **- hydration, early feedings, phototherapy
Pre term
Late preterm
Full term
Post term
Pre term - before 37 wks
Late preterm - 34 0/7 - 36 6/7
Full term - 38-41wks
Post term - 42 wks +
After 42 weeks placenta begins aging, what happens
Deposits of fibrin and calcium along with hemorrhagic infarcts occur and placental blood vessels begin to degenerate
Wasting occurs, loss of subQ and muscle
Newborn respiratory system
Surfactant deficiency leads to
Unstable chest wall leads to
Immature respiratory control centers leads to
SMaller respiratory passages leads to
Inability to clear fluid from passages leads to
Surfactant deficiency leads to develop of respiratory distress syndrome
Unstable chest wall leads to atelectasis
Immature respiratory control centers leads to apnea
SMaller respiratory passages leads to increased risk for obstruction
Inability to clear fluid from passages leads to transient tachypnea
What is it called when a newborn fails to establish adequate sustained respiration after birth
Asphyxia (perinatal acidosis)
_Depirvation of oxygen during birth process resulting in hypoxia that can lead to organ damage and death
Equiptment for newborn resuscitation
- Wall vaccum suction
- Stethoscope
- pulse ox
- epinephrine
- volume expander
- IV fluids
- Wall or tank of 100% o2 w/ flow meter
- self inflating ventilation bag
- endotracheal tubes
- laryngoscopre
- ampules of naloxone w/ syringes
- wall clock
- disposable gloves
large concentrations of 02 and sustained o2 sat higher than 95% while on supplemental ox have been assoc with
retinopathy of prematurity and further respiratory complications
*commone practice is to maintain o2 high 80s-mid 90s
*room air is perferred gas
When newborn becomes chilled it attempts to conserve body heat by
vasoconstriction and thermogenesis by metabolizing brown adipose tissue and increasing o2 consumption
What are symptoms of a newborn who is having problems with thermal regulation
Cool - cold touch
cyanotic
shallow or slow respirations
lethargic, hypotonic
feeds poorly
feeable cry
hypoglycemia
Complications of hypothermia in newborn
Metabolic acidosis (secondary to anerobic metabolism used for heat production results in production of lactic acid)
Hypoglycemia
Pulmonary htn (secondary to pulmonary vasoconstriction)
Signs of hyperthermia in newborn
tachycardia, tachypnea, apnea, warn to touch, flushed skin, lethargy, weak or absent cry, CSN depression
What are different methods to admin newborn feedings
-Parenteral
-Enteral
Before34 weeks?
After 34 weeks?
Parenteral - through percutaneous central venous catheter delivery of TPN
Enteral - oral, continous nasogastric tube, or intermittent gavage tube feedings
After 34 wks - orally
Before 34 wks - parenteral
What are some common indicators of pain in a newborn
facial expression, cry, withdrawl of body part, total body movment, physiological changes (o2 sat and rr)
define asphyxia
impairment in gas exchange resulting in a decrease in blood oxygen levels (hypoxemia) and excess of carbon dioxide or hypercapnia that leads to acidosis
What are risk factors to look for for hypoxic-ischemic encephalopathy?
Trauma from birth
Interuterine asphyxia
Sepsis
Malformation
Hypovolemic shock
Medication (hypnotics, excessive oxytocin, analgesics, narcotics)
For newborn resuscitation, continue until what signs?
Pulse above 100bpm
good healthy cry
good breathing efforts
pink tounge (indicates good o2 supply to brain)
AAP suggests stopping resuscitation if newborn exhibits no decetable heart rate after —-mins
10mins
Reperfusion injury
when normal oxygenation and blood flow are restored too quickly - can cause inflammation
What does surfactant do
forms a coating over the inner surface of alveoli, reducing surface tension and preventing alveolar collarpse at end of expiration
What are the parameters assessed for the silverman-Anderson index?
Retractions of upper chest
Lower chest
Xiphoid
nasal flaring
expiratory grunt
0 - normal
1-moderate impairment
2- severe
What treatment do you administer if a newborn has worsening hypoxemia and acidosis from meconium aspiration?
Hyperoxygenation to dilate pulmonary vasculature and close ductus arteriosis
OR
Nitric oxide inhalation to decrease pulm vasc resistance
OR
High freq oscillatory ventilation to increase chance of air trapping
In addition, admin vasopressor and pulm vasodilators along with surfactant
Where is periventricular area
Rim of brain tissue that lines the outside of lateral ventricles
Contains rich network of capillaries that are extremely fragile and can rupture easily
What will the lab tests ordered for Necrotizing Enterocolitis tell us
Kideny, ureter, bladder Xray
Ab XRAY
Blood values
Kideny, ureter, bladder Xray - confirms presence of pneumatosis intestinalis (air in bowel wall) and persistenly dialted loop of bowel
Ab XRAY - dilated bowel loops, abnormal gas patterns, air bubbles from bacteria adn thickened bowel walls
Blood values- metabolic acidosis, increased WBC, thrombocytopenia, neutropenia, electrolyte imbalance, DIC
Infants of DM moms w/ vascular disease seldom develop RDS bc
the chronic stress of poor intrauterine perfusion leads to increased production of steroids which accelerates lung maturation
What are the characteristics of a newborn to a DM mom
Puffy, rose cheeks
SHort neck
Buffalo hump
Massive shoulders
Distended upper ab
Excessive subQ fat
How to prevent hypoglycemia with early feedings.. Benefits
provide early feedings (w/in 1 hr of birth)
feedings help to control glucose levels, reduce hematocrit adn promote bilirubin excrettion
How to monitor blood glucose on a newborn? how often
heel stick q hour for first 4 hrs
then every 3-4 hrs until stable
In a brachial plexus injury what reflexes are present/absent
present - grasp
Absent - moro, bicep and radial
Cephalohematoma
Collection of blood secondary to rupture if vessels between skull and periosteum.
Appears w/in hours after birth
Caput succedaneum
soft tissue swelling caused by edema of head against dilating cervix during birth
Subarachnoid hem
may be due to hypoxis-ischemia, variations in BP, and pressure on head during labor
Bleeding of venous orign and contusions may also occur
Subdural hem
(hemtomas)
tears of major veins overlying cerebral hemispheres or cerebellum. Increased pressure leads to tears
Depressed skull fractures
may result from forceps, can also be spontaneous. causing subdural bleed, subarachnoid hem or brain trauma
What 3 specific findings are a pattern of FAS
- Growth restriction
- carniofacial structural abnormalities
- CNS dysfunction
What is the clinical picture of FAS
Microcephaly
Small eyelid fissures
abnormally small eyes
FGR
Maxillary hypoplasia
Thin upper lip
Short upturned nose
low birth weight
joint and limb defects
SGA
Congential cardiac defects
delayed fine and gross motor develop
poor eye-hand coord
mentally challanged
narrow forehead
Inadequate sucking and poor appetite
Manifestations of Neonatal abstinence syndrom
CNS
METABOLIC, VASOMOTOR, RESPIRATORY
GI
CNS
Tremors, irritability
Seizures, hyperactive reflex, restlessness
Exaggerated moro., hypertonic, constant movment
high pitched excessive cry, disturbed sleep
Metabolic
Fever, freq yawning, mottling of skin, sweating, sneezing, nasal flaring, trachypnea 60+. apnea
GI
Poor feeding, frantick sucking, loose stools, projectile vomit
What 3 mechanisms does bilirubin rise in newborns
Increased production RBC
Decreased removal (transient liver enzyme insufficency)
increased reabsorbtion (delay in bowels)
What does physiologic jaundice result from
increased bili load bc of relative polycythemia, shortend RBC life span, immature hepatic uptake and conjugation process, increased enterohepatic circulation
*delayed passage of meconium are more likely to have
Acute bilirubin encephalopathy
effects of hyperbili in first few weeks
can lead to death
Lethary, poor feeding, high pitched cry, poor tone, poor moro, incomplete flexion / as symptoms worsen = apnea, seizures, coma and death
Chronic bili encephalopathy
aka Kernicterus
preventable neurologic syndrome resulting from deposition of unconjugated (indirect) bili in basal ganglia and brainstem nuclei
Movement disorder, auditory dysfunction, oculomotor impairment, dental enamel hypoplasia of deciduous teeth
What are clinical manifestations of newborn Rh incompatibiltiy
ascites, anemia, CHF, edema, pallor, jaundice, hepatosplenomegaly, polyhydramnios, thick placenta, dialtion of umbilical vein
What do the following test tell us
Direct Coombs test
Hemoglobin concentration
Total serum protein
Reticulocyte count
**Direct Coombs test **- id hemolytic disease (positive indicated sensitized)
Hemoglobin concentration - anemia
Total serum protein - Rh status and incompatibilty
Reticulocyte count - Id elevated level indicating increase hemolysis
What are the signs of organ system dysfunction
Cardio compromise
Respiratory compromise
Renal compromise
Systemic compromise
Cardio compromise - tachycardia and hyptenson
Respiratory compromise - respiratory distress and tachypnea
Renal compromise - oliguria or anuria
Systemic compromise - abnormal values
DIfference between gastroschisis and omphalocele
GASTROSCHISI- eviscerated bowel without peritoneal covering
OMPHALOCELE - eviscerated bowel with peritoneal covering
